ArticleOncogene2000
Ovarian cancer cells that coexpress endogenous Rb and p16 are insensitive to overexpression of functional p16 protein.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 33 citations in OpenAlex.
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- Comprehensive Analysis Revealed thatFrontiers in cell and developmental biology · 2021Article
- Oncolytic adenovirus shapes the ovarian tumor microenvironment for potent tumor-infiltrating lymphocyte tumor reactivity.Journal for immunotherapy of cancer · 2020Article
- On-chip immunofluorescence analysis of single cervical cells using an electroactive microwell array with barrier for cervical screening.Biomicrofluidics · 2019Article
- Doxycycline-Regulated p16Journal of Cancer · 2017Article
- Comparative analysis of Rb1, P16 and ER as diagnostic, prognostic and potential targets for therapeutic agents in ovarian epithelial tumors: an immunohistochemical study of 130 ovarian carcinomas.Journal of ovarian research · 2015Article
- Pathway modulations and epigenetic alterations in ovarian tumorbiogenesis.Journal of cellular physiology · 2014Review
- Identifying microRNA/mRNA dysregulations in ovarian cancer.BMC research notes · 2012Article
- Altered p16(INK4) and RB1 Expressions Are Associated with Poor Prognosis in Patients with Nonsmall Cell Lung Cancer.Journal of oncology · 2012Article
- Effects of p16 gene on biological behaviours in hepatocellular carcinoma cells.World journal of gastroenterology · 2003Article
- Adenovirus-mediated N5 gene transfer inhibits tumor growth and metastasis of human carcinoma in nude mice.Cancer gene therapy · 2002Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Defects of the 'Rb/cyclin D1/p16 pathway' have been shown to play a critical role in the development of virtually all human malignancies assessed. To determine the contribution of G1 phase cell cycle defects to ovarian tumorigenesis, we have examined a panel of normal and tumor ovarian tissues and ovarian cancer cell lines for the expression of Rb, p16 and cyclin D1 proteins. Unlike most types of human cancer whose development involves the loss of either Rb or p16 expression, we observed the coexpression of Rb, p16 and cyclin D1 in 82% of ovarian cancer tissues and cell lines. Furthermore, the growth and cell cycle distribution profiles of three ovarian cancer cell lines (ES-2, PA-1 and NIH OVCAR-3) that coexpressed Rb and p16, were found to be unaffected by adenoviral-mediated overexpression of functional p16 protein, indicating the existence of a defect(s) downstream from p16 in these cells. By contrast overexpression of ectopic p16 in the one ovarian cancer cell line (SK-OV-3) that expressed Rb but lacked p16 protein, resulted in a G1 growth arrest. These data suggest that defects of the 'Rb/cyclin D1/p16 pathway', other than the loss of Rb or p16, may play a major role in the development of ovarian cancer.
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